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However, transfer of RANTES and IP-10 conditioned CFP10-DCs induced effective and significant reduction in the bacterial loads in both lungs and spleen.
B. burgdorferi producing OspC with 5-AA deletion was able to generate similar bacterial loads in both joint and skin tissues of SCID mice as the control, indicating that the truncated OspC can effectively protect the pathogen against innate immune clearance at least in these tissues.
One sample (UT530) was a clear outlier, both for buffy coat and isolation quantitation, as it demonstrated high bacterial loads in both samples; 28 237/μL of buffy coat and 1 059 061/μL of VERO cell culture at 100% infection of cells as determined by IFA.
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This suggests that the magnitude of differences in bacterial burdens for lungs among the groups is not the same from round 1 to round 2. As shown in Figure 3, our results indicated that the mean bacterial load in both blood and spleen was statistically highest in type B infected mice.
Secondly, we wanted to model and provide estimates of MRSA bacterial load in both species.
Genotype was a strong predictor of Bacterial Load in both the acute and chronic phase of infection (Model E; Table 5; Genotype: p < 0.001), clearly demonstrating genetic variation for resistance.
This was associated with decreased host clearance capacity reflected in enhanced bacterial load in both the spleen and the joint and was accompanied by enhanced detection of microbial antigens in the synovial tissues by immunohistological staining.
Thus, although we have genetic variation for bacterial load in both the acute and chronic phase of infection, the impact of this burden on fitness differs dramatically between the two phases of infection.
At 16 hpi, the bacterial load in the spleen (104 CFU/organ) was significantly higher than the liver (103 CFU/organ) (p-value = 0.0009) while the bacterial load in both organs were similar at 24 hpi and 42 hpi, with an average of 104 to 105 CFU/organ.
Whereas the bacterial burdens were not significantly different between TLR2 KO and WT mice 24 h post infection, at 48 and 72 h TLR2 KO displayed significantly higher bacterial loads in their lungs than WT mice (both P < 0.05).
There were no differences in bacterial loads in lung, blood or spleen between the groups at both time points.
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